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  3. Conserved Cell-type-specific Transcriptomic Networks And Regulatory Programs Underlie Alcohol Dependence Across Mouse And Human.
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  3. Conserved Cell-type-specific Transcriptomic Networks And Regulatory Programs Underlie Alcohol Dependence Across Mouse And Human.

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Conserved Cell-Type-Specific Transcriptomic Networks and Regulatory Programs Underlie Alcohol Dependence Across Mouse

Nihal Salem1,2, Anna Warden1,2, Amanda Roberts3

  • 1Waggoner Center for Alcohol and Addiction Research, The University of Texas at Austin, Austin, TX 78712, USA.

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|May 4, 2026

View abstract on PubMed

Summary
This summary is machine-generated.

Researchers identified shared molecular signatures of alcohol use disorder (AUD) across mouse models and humans. This cross-species analysis highlights conserved gene networks and upstream regulators in specific brain cells, offering new therapeutic targets for AUD.

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Area of Science:

  • Neuroscience
  • Genetics
  • Pharmacology

Background:

  • Alcohol use disorder (AUD) is a complex polygenic disease.
  • Rodent models and single-nucleus transcriptomics are key tools for studying AUD.
  • Cell-type-specific gene expression changes are crucial in understanding AUD.

Purpose of the Study:

  • To identify shared dysregulated transcriptomic networks (TN) in a mouse model of alcohol dependence and human AUD.
  • To pinpoint cell-type-specific molecular signatures conserved across species.
  • To discover upstream regulators of alcohol-dysregulated genes for translational research.

Main Methods:

  • Comparative analysis of transcriptomic networks (gene co-expression and regulatory networks) between mouse models and human AUD data.
  • Cell-type-specific network analysis using single-nucleus transcriptomics.
  • Integration of human and mouse gene regulatory network data to identify transcription factors.

    • Main Results:

    • Identified conserved, dependence-upregulated gene co-expression modules in astrocytes (hub gene Slc1a3) and oligodendrocytes (hub gene Pde4b).
    • Discovered shared upstream transcription factors (e.g., Mef2a, Jund, Nr3c1) regulating alcohol-dysregulated genes in both species.
    • Highlighted conserved molecular signatures relevant to glutamate signaling and PDE4 inhibition.

    Conclusions:

    • Cross-species, cell-type-specific network analysis effectively uncovers conserved molecular mechanisms in alcohol dependence.
    • Identified shared networks, cell type homologies, and upstream regulators provide a foundation for translational therapeutic strategies.
    • Findings support the development of targeted interventions for AUD based on conserved molecular pathways.